Mutations such as KRAS G12C, G12D, and G12V drove the reprogramming of macrophages into protumor TAMs, with a significantly greater effect compared to wild‐type KRAS.[52] Mechanistically, oncogenic KRAS signaling enabled immune evasion in lung adenocarcinoma by activating CD47.[53] KRAS mutations increased reactive oxygen species (ROS) production, which stabilizes HIF‐1α, thereby promoting the production of CSF2 and lactate by tumor cells. The gene discussed is KRAS; the disease is lung adenocarcinoma.